This invention relates to devices substituting for or assisting the heart, either corporally or extracorporally.
The blood supply to the heart muscle occurs via the coronary circulation. Defects in this area of the circulatory system are among the most common afflictions of mankind. When an increased amount of work is required of the heart, an increase in coronary blood flow must occur to provide for the additional oxygen requirements of the muscle fibers. The vessels in the coronary system differ from those in most of the rest of the body in that the major branches lie within contracting muscle fibers. External pressure by the myocardium during ventricular systole compresses the vessels and decreases blood flow, even though the aortic pressure is increased, 70 percent of the coronary arterial flow therefore occurs during diastole. Compression of the vessels, however, hastens the discharge of venous blood due to squeezing on the veins. Outflow from the coronary veins is therefore greater in systole than in diastole.
The left coronary artery supplies most of the left ventricle and the anterior portion of the ventricular septum. The right coronary artery supplies the right ventricle and the posterior portion of the septum. Since the left coronary artery supplies a large portion of the left ventricle, occlusion of a major branch generally seriously damages the pumping ability of this high pressure chamber. The right coronary arterial system on the other hand, supplies a chamber that needs to produce only low pressures and may suffer considerable damage without significant impairment of its pumping ability. Branches from the right coronary system supply the SA (sino-atrial) and AV (atrio-ventricular) nodal areas, however, and damage to these areas may produce life-threatening arrhythmias. In terms of relative flow distribution, about 85 percent of total coronary blood flow occurs through the left coronary artery and about 15 percent through the right coronary artery. Most of the venous return from the left coronary artery occurs through the great coronary vein into the coronary sinus in the right atrium; from the right coronary artery, venous return is via the anterior cardiac vein to the right atrium.
Cardiac muscle, like smooth muscle, skeletal muscle, and nerve, possesses a resting electrical potential relative to the ion distribution across the cell membrane. Like these tissues, it also has the ability to depolarize; depolarization (and repolarization) is manifested by a change in the electrical potential across the cell membrane. Most of the areas of the heart can depolarize spontaneously and thereby can contract without external nerve stimulation. This property of myocardial tissue is termed automaticity. Normally, the depolarization and repolarization processes proceed in an orderly fashion through the heart tissue, producing a characteristic electrocardiographic pattern. The SA node, a group of specialized muscle cells derived from the area of junction of the embryonic sinus venosus and the atrium, lies at the junction of the right atrium and the superior vena cava. These cells tend to depolarize spontaneously faster than those in any other area of the heart. Hence they normally control the heart rate and are called pacemaker cells. If for some reason this area fails to be the most rapidly depolarizing, the pacemaker site shifts to other areas, such as the AV node, which lies at the lower posterior, right side of the atrial septum and gives rise to a group of specialized muscle fibers.
All of these specialized muscle cells have the property of automaticity and serve to conduct the electrical impulse rapidly through the heart.
Once the cell potential reaches threshold, the characteristic rapid action potential is produced. This action potential spreads out from the SA node over the surface of the atria, activating the normally quiescent atrial cells. These cells in turn depolarize, and the impulse is thus passed to the AV nodal area. The specialized cells in the AV node repond poorly, and conduction through this area is very slow. In some cases the impulse may not get through at all, resulting in a dropped beat or a shift to another pacemaker site. Normally, however, after a short delay, the impulse spreads out to activate the ventricular muscle. The action potentials of the conduction bundles and ventricular muscle cells differ from those of the pacemaker and atrial areas in possessing a long plateau phase of depolarization. During this time the cell cannot be stimulated by another incoming action potential. This plateau phase lasts until the muscle contraction has been completed. Thus, unlike skeletal muscle, cardiac muscle cannot show tetanic contraction. This refractory abililty is important in the heart's action as a mechanical pump to allow adequate time for filling to occur.
Various abnormalities in the electrical activity of the heart resulting from damage to the SV or AV nodal areas are a primary cause of ineffectual contraction of the heart and subsequent death. Representative arrhythmias include a rapid, but regular, atrial rate (atrial tachycardia), which in some instances may be associated with a premature beat, before the normal diastolic time interval has passed, resulting in an earlier and usually less effective ventricular beat. In atrial flutter and atrial fibrillation the atrial rate is even more rapid. Flutter refers to a condition in which a rapid depolarization of the right atrium appears to occur in a circle around its junction with the superior and interior vanae cavae (circus depolarization); the resultant wave of electrical depolarization spreads out over the surface of the atria, causing rapid atrial contraction. Fibrillation refers to an even faster rate, in which there is not coordinated activity; rather, it appears that each small area of the muscle has a circus movement of its own, thereby producing no effectual contraction. In atrial fibrillation, the atrial rate is so fast that the ventricles respond at totally irregular times to an occasional impulse passing through the AV node.
The ventricular rate may not be the same as the atrial rate; i.e., the atrial beat may not be propagated through the AV node to the ventricle, or, contrariwise, the ventricle may initiate extra beats. If the beat originates in the ventricles, the resultant pattern of depolarization is abnormal. Ventricular premature beats or premature ventricular contractions (PVC's), are instances in which a single beat--or a short run of beats--occurs abnormally from a ventricular pacemaker site. If the ventricle is still in a depolarized state when the next atrial depolarization wave reaches it, there will be no response, and a compensatory pause will occur until the second normal atrial beat arrives. Rapidly firing ventricular sites produce ventricular tachycardia, an extremely dangerous condition, which may progress to ventricular fibrillation. In this condition no coordinated contraction occurs, and thus there is no effecting pumping of blood. This may be treated effectively only by electrically polarizing the entire heart muscle (defibrillating) and hoping to restart it from a single pacemaker site.
While advances in medical science have succeeded in counteracting some effects of such abnormalities, devices such as pacemakers have proved not entirely effective in regulating cardiac contractions, and are known in some instances to actually induce ventricular fibrillation. Further, heart transplants have had disappointing results, and are also extremely expensive.